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  • 1
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    Positive regulation of T cell activation and integrin adhesion by the adapter Fyb/Slap (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-22
    Description: The molecular adapter Fyb/Slap regulates signaling downstream of the T cell receptor (TCR), but whether it plays a positive or negative role is controversial. We demonstrate that Fyb/Slap-deficient T cells exhibit defective proliferation and cytokine production in response to TCR stimulation. Fyb/Slap is also required in vivo for T cell-dependent immune responses. Functionally, Fyb/Slap has no apparent role in the activation of known TCR signaling pathways, F-actin polymerization, or TCR clustering. Rather, Fyb/Slap regulates TCR-induced integrin clustering and adhesion. Thus, Fyb/Slap is the first molecular adapter to be identified that couples TCR stimulation to the avidity modulation of integrins governing T cell adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffiths, E K -- Krawczyk, C -- Kong, Y Y -- Raab, M -- Hyduk, S J -- Bouchard, D -- Chan, V S -- Kozieradzki, I -- Oliveira-Dos-Santos, A J -- Wakeham, A -- Ohashi, P S -- Cybulsky, M I -- Rudd, C E -- Penninger, J M -- New York, N.Y. -- Science. 2001 Sep 21;293(5538):2260-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11567140" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD/metabolism ; Antigens, CD3/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; B-Lymphocytes/immunology ; Carrier Proteins/genetics/*physiology ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Chimera ; Gene Targeting ; Humans ; Immunization ; Immunoglobulin G/biosynthesis ; Integrins/*metabolism ; Intercellular Adhesion Molecule-1/metabolism ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis/pharmacology ; Lectins, C-Type ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Phosphoproteins/genetics/*physiology ; Receptors, Antigen, T-Cell/immunology/metabolism ; Receptors, Interleukin-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/metabolism/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Mimicry of CD40 signals by Epstein-Barr virus LMP1 in B lymphocyte responses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: The effect of the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) on the activation and differentiation of normal B cells was investigated. B cells of transgenic mice expressing LMP1 under the control of immunoglobulin promoter/enhancer displayed enhanced expression of activation antigens and spontaneously proliferated and produced antibody. Humoral immune responses of LMP1 transgenic mice in CD40-deficient or normal backgrounds revealed that LMP1 mimics CD40 signals to induce extrafollicular B cell differentiation but, unlike CD40, blocks germinal center formation. Thus, these specific properties of LMP1 may determine the site of primary B cell infection and the state of infection in the natural course of EBV infection, whereas subsequent loss of LMP1 expression may affect the site of persistent latent infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uchida, J -- Yasui, T -- Takaoka-Shichijo, Y -- Muraoka, M -- Kulwichit, W -- Raab-Traub, N -- Kikutani, H -- CA19014/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):300-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514374" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; Antigens, CD40/genetics/*metabolism ; B-Lymphocytes/*immunology/metabolism/virology ; Cell Differentiation ; Female ; Germinal Center/immunology/metabolism ; Herpesvirus 4, Human/*metabolism/physiology ; Immunization ; Immunoglobulin Class Switching ; Immunoglobulins/biosynthesis ; Interleukin-4/pharmacology ; *Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Molecular Mimicry ; NF-kappa B/metabolism ; Signal Transduction ; Spleen/immunology ; Viral Matrix Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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